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Ethanol extract of the Pinus koraiensis leaves anti-obesity and hypolipidemic effects by inhibiting adipogenesis and activating the AMPK signaling Myoung-Sun Leea, Sun-Mi Choa, Myeong-Ok Kima, Joo-Seok Kima, Min-ho Leeb, Eun-Ok Leea, Sung-Hoon Kima, Hyo-Jeong Leea,* a Korea Cancer Preventive Material Development Research Center, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-gu, 130-701, Seoul, Republic of Korea, b College of health industry, Eulji University, Seongnam, 461-713, Seoul Republic of Korea Pinus koraiensis from family Pinaceae is an evergreen tree found in Korea, China and far eastern Russia. In this study, we investigated the anti-obesity and anti-hyperlipidemic mechanism of the ethanol extract of Pinus koraiensis leaves (EPK) using in vitro and in vivo model. EPK significantly decreased lipid accumulation and intracellular triglyceride in the differentiated 3T3-L1 adipocytes. EPK treatment suppressed expression of adipogenic transcription factors including peroxisome proliferator-activated receptor-š¯›¾ (PPARš¯›¾) and CCAAT/enhancer-binding proteins š¯›¼ (C/EBPš¯›¼). In addition, EPK suppressed the expression of FABP and GPDH in the differentiated 3T3-L1 adipocytes. Remarkably, The EPK upregulated phosphorylation of AMPK (p-AMPK). Further studies demonstrated that the antiadipogenic effect of EPK was reversed by the AMPK siRNA. In vivo study, body weight gain, serum triglyceride, total cholesterol, low-density lipoprotein (LDL) cholesterol and atherosclerosis index (AI) value in the 100 or 200 mg/kg of EPK treatment group were decreased, when compared to high-fat diet (HFD) control group. Consistently, EPK increased high-density lipoprotein (HDL) cholesterol in a dose-dependent manner. Immunohistochemistry and western blotting analysis revealed that EPK inhibited the expression of PPARš¯›¾ and induced the expression of p-AMPK in the liver tissue and adipose tissue of EPK-treated rats. Through activity-guided isolation of bioactive constituents with anti-adipogenic activity from EPK, Lambertianic acid (LA) was identified and, inhibited fat accumulation in adipocyte. Further, LA induced the expression of p-AMPK and inhibited PPARš¯›¾. In summary, these results suggest that EPK were anti-obesity potential by AMPK and PPARš¯›¾-related signaling. References [1] Steinberger, J., Daniels, S. R., American Heart Association Atherosclerosis, H., Obesity in the Young, C., and American Heart Association Diabetes, C. (2003) Obesity, insulin resistance, diabetes, and cardiovascular risk in children: an American Heart Association scientific statement from the Atherosclerosis, Hypertension, and Obesity in the Young Committee (Council on Cardiovascular Disease in the Young) and the Diabetes Committee (Council on Nutrition, Physical Activity, and Metabolism), Circulation 107, 1448-1453. [2] Wing, R. R., and Jeffery, R. W. (1995) Effect of modest weight loss on changes in cardiovascular risk factors: are there differences between men and women or between weight loss and maintenance?, Int J Obes Relat Metab Disord 19, 67-73. [3] Caro, J. F., Dohm, L. G., Pories, W. J., and Sinha, M. K. (1989) Cellular alterations in liver, skeletal muscle, and adipose tissue responsible for insulin resistance in obesity and type II diabetes, Diabetes Metab Rev 5, 665-689. Keywords: Ethanol of Pinus koraiensis, 3T3-L1 adipocytes, anti-obesity, peroxisome proliferator- activated receptor-Ī³, CCAAT/enhancer-binding proteins Ī±